[Clinical value of TNF, IL-6, and IL-10 gene polymorphic markers in chronic glomerulonephritis].

AIM: To study the association of the polymorphic markers (PMs) G(-238)A of the TNF gene, G(-174)C of the IL-6 gene, and G(-1082)A of the IL-10 gene with the clinical characteristics of chronic glomerulonephritis (CGN) and a response to immunosuppressive therapy (IST). SUBJECTS AND METHODS: Clinical syndromes at the time of diagnosis, the morphological types of nephritis, and a response to IST were analyzed in relation to the carriage of the examined PMs of the TNF, IL-6, and IL-10 genes in 102 patients with CGN. RESULTS: No association was found between the PM G(-238)A of the TNF gene and the clinical features of CGN. The carriers of the C allele of the PM G(-174) C of the IL-6 gene versus the homozygous individuals were observed to have more frequently kidney dysfunction at the time of diagnosis (р=0.014). Hypertension was more common in the carriers of the AA genotype of the PM G(-1082)A of the IL-10 gene (p=0.023); moreover, they tended to have a more frequent concurrence of nephrotic syndrome and hypertension (p=0.082). Analysis of the distribution of the morphological types of CGN disclosed that the proliferative variants were more common in the patients with the GG genotype (the TNF gene) as compared to the A allele carriers (p=0.067); and the nonproliferative forms were in the individuals homozygous for GG (the IL-6 gene) as compared to the C allele carriers (p=0.067). Examination of an IST response showed that a complete response at 12 months of treatment occurred more frequently in the carriers of the C allele of the IL-6 gene (p=0.045) and in those of the GG genotypes of the IL-10 gene (p=0.030). CONCLUSION: There was an association of the PMs G(-174)C of the IL-6 gene and G(-1082)A of the IL-10 gene with the clinical features of CGN and a response to IST.

[NEWLY-DIAGNOSED CHRONIC KIDNEY DISEASE IN PATIENTS OF A THERAPEUTIC CLINIC: THE ROLE OF GFR CALCULATION BY THE CKD-EPI FORMULA].

AIM: to estimate the prevalence of newly-diagnosed chronic kidney disease (CKD) and its risk factors in patients of a therapeutic clinic, to evaluate the importance of GFR calculation using the CKD-EPI formula. Materials and methods: the study included 275 patients (275 (31.1%) men and 610 (68.9%) women) aged 18-89 (mean 59.5 13.95) years. GFR of 60ml/min/l.73 m3 or signs of kidney lesions were diagnosed as CKD. Possible risk factors of CKD were elucidated based on the results of a questionnaire that provided information on complaints, metabolic disorders, family histoty compliance with a healthy lifestyle. Arterial pressure and serum creatinine level were measured, BMI and GFR calculated in all patients. RESULTS: Medical histories of 58% of the 885 patients contained signs of CKD. Among the remaining 372 (42%) ones, 7.2% had proteinuria and 20.1% GFR of 60ml/min/1. 73/m3. The prevalence of newly diagnosed CKD was 27.3%. The use of the CKD-EPI formula allowed to diagnose CKD in 18% of the patients having the serum creatinine level within normal values. The overall prevalence of CKD in the study group was 14%. CONCLUSION: the prevalence of newly diagnosed CKD in patients of a therapeutic clinic was 2 7.3%. The use of the CKD-EPI formula facilitates diagnostics of CKD.

[Urinary excretion of angiogenesis regulatory factors and renal injury markers in chronic glomerulonephritis: Significance in the assessment of progression].

AIM: To study the urinary excretion of the molecular factors regulating angiogenesis, such as vascular endothelial growth factor type A (VEGF-A), thrombospondin 1 (THBS1), and angiopoietin 2 (ANGPT2), versus that of the urinary markers of renal injury and fibrogenesis, such as neutrophil gelatinase-associated lipocalin (NGAL), type IV collagen (COL4), and known clinical risk factors for accelerated disease progression to estimate the prognostic value of urinary excretion in patients with chronic glomerulonephritis (CGN). SUBJECTS AND METHODS: Eighty-two patients (45% men, 55% women; mean age, 36.5 years) with a clinical diagnosis of CGN were examined. 31.7% of the examinees presented with nephrotic syndrome; 31.7% had a glomerular filtration rate (GFR) of less than 60 ml/min/1.73 m2. Morning urine samples were analyzed by Elisa to determine the urinary excretion of biomarkers (VEGF-A, THBS1, ANGPT2, NGAL, and COL4). The results were adjusted to urinary creatinine concentrations. RESULTS: The urinary excretion of the angiogenesis regulators VEGF-A, THBS1, and ANGPT2 correlated between them, with that of the renal injury markers NGAL and COL4, with the level of proteinuria. That was found to be unassociated with blood pressure and GFR. In the presence and absence of nephrotic syndrome, high (> 75th percentile) urinary excretion rates were 46.2 and 14.8% for VEGF-A (p < 0.01); 50 and 13% for THBS1 (p < 0.001); and 46.2 and 14.8% for ANGPT2 (p < 0.01), respectively. That for ANGPT2 was also high in the presence of anemia (63.2 versus 11.7%; p < 0.001). CONCLUSION: The finding of the high urinary excretion of the angiogenesis regulators VEGF-A, THBS1, and ANGPT2 and its association with that of kidney injury markers in the patients with the proteinuric forms of CGN suggest that this excretion may be considered as an integral index that displays glomerular injury and indicates tubulointerstitial proteinuric/hypoxic remodeling.